scholarly journals Quantitative Nano‐Amperometric Measurement of Intravesicular Glutamate Content and of its Sub‐Quantal Release by Living Neurons

Author(s):  
Xiao-Ke Yang ◽  
Fu-Li Zhang ◽  
Wen-Tao Wu ◽  
Yun Tang ◽  
Jing Yan ◽  
...  
2021 ◽  
Author(s):  
Xiao-Ke Yang ◽  
Fu-Li Zhang ◽  
Wen-Tao Wu ◽  
Yun Tang ◽  
Jing Yan ◽  
...  

2021 ◽  
Vol 27 (S1) ◽  
pp. 500-502
Author(s):  
Oleg Suchalko ◽  
Roman Timoshenko ◽  
Alexander Vaneev ◽  
Vasilii Kolmogorov ◽  
Nikita Savin ◽  
...  

Neurology ◽  
2006 ◽  
Vol 66 (8) ◽  
pp. 1223-1229 ◽  
Author(s):  
M. Milone ◽  
T. Fukuda ◽  
X. M. Shen ◽  
A. Tsujino ◽  
J. Brengman ◽  
...  

ChemBioChem ◽  
2018 ◽  
Vol 19 (23) ◽  
pp. 2458-2464 ◽  
Author(s):  
Isam Elamri ◽  
Maximilian Heumüller ◽  
Lisa‐M. Herzig ◽  
Elke Stirnal ◽  
Josef Wachtveitl ◽  
...  
Keyword(s):  

Neuron ◽  
2003 ◽  
Vol 38 (1) ◽  
pp. 89-101 ◽  
Author(s):  
Michael A Freed ◽  
Robert G Smith ◽  
Peter Sterling

1983 ◽  
Vol 63 (3) ◽  
pp. 915-1048 ◽  
Author(s):  
M. R. Bennett

Quantal secretion at nerve terminals in mature muscles depends on the number of terminal branches and the size of release sites (sect. VB4). The physical length of SBL determines the length of terminal branch that can be laid down in a reinnervation experiment (sect. IVA4). A limit is set on the total length of terminal branches formed by a motoneuron; this limit is determined by the amount of TF (sect. IVB) made available from the neuron soma to the peripheral branches of the neuron (sect. VC). As a result of this limit, not all SBL needs to be occupied at a site by terminal branches. The SBL eventually disappears if it is not occupied by terminal branches (sect. IVA2). If a muscle is relatively inactive, it synthesizes and releases at synaptic sites additional amounts of NGF, which stimulates the growth of additional terminal branches. These may secrete sufficient amounts of AF to induce the formation of new SRs with associated SBL. In these circumstances a new synaptic site is formed or an extension of an existing site is created. If the size of a motor unit is decreased, the enhanced release of TF at the remaining terminals ensures that each occupies all the SBL at the synaptic site. Furthermore the enhanced release of AF per terminal induces more SBL, allowing additional terminal branches on the muscle cells to be established. Neither of these changes occurs unless the threshold amount of NGF is available from the muscle to stabilize the terminals. If this condition is met, an increase in quantal release per terminal occurs after reducing the size of a motor unit (sect. VC). An increase in quantal release per terminal also occurs after inactivation of a muscle. Such inactivation leads to an enhanced release of NGF per synaptic site (sect. VA4). Extra terminals may then form if sufficient TF is available; these may innervate existing but empty synaptic sites. In rare circumstances the extra terminal may induce SBL and innervate these new sites if sufficient AF is available. In both cases the quantal release per terminal increases. During development the secretory capacity of the axon terminal depends on the muscle cells with which it synapses. This secretory capacity can be enhanced either by increasing the number of terminal branch pairs or by increasing the secretory capacity of individual release sites. If two terminals innervate a synaptic site, their individual secretory capacity is reduced--in these circumstances the terminal's secretory capacity depends on the amount of NGF available to the terminal; two terminals must share their NGF.


2012 ◽  
Vol 198 (2) ◽  
pp. 251-263 ◽  
Author(s):  
Enora Moutin ◽  
Fabrice Raynaud ◽  
Jonathan Roger ◽  
Emilie Pellegrino ◽  
Vincent Homburger ◽  
...  

Scaffolding proteins interact with membrane receptors to control signaling pathways and cellular functions. However, the dynamics and specific roles of interactions between different components of scaffold complexes are poorly understood because of the dearth of methods available to monitor binding interactions. Using a unique combination of single-cell bioluminescence resonance energy transfer imaging in living neurons and electrophysiological recordings, in this paper, we depict the role of glutamate receptor scaffold complex remodeling in space and time to control synaptic transmission. Despite a broad colocalization of the proteins in neurons, we show that spine-confined assembly/disassembly of this scaffold complex, physiologically triggered by sustained activation of synaptic NMDA (N-methyl-d-aspartate) receptors, induces physical association between ionotropic (NMDA) and metabotropic (mGlu5a) synaptic glutamate receptors. This physical interaction results in an mGlu5a receptor–mediated inhibition of NMDA currents, providing an activity-dependent negative feedback loop on NMDA receptor activity. Such protein scaffold remodeling represents a form of homeostatic control of synaptic excitability.


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